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Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Inhibition of CDK Activity

Inhibition of CDK Activity

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

M-Cdk Drives Transition Into Mitosis

M-Cdk Drives Transition Into Mitosis

Negative Regulator Molecules

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

Positive Regulator Molecules

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

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Related Experiment Video

Updated: Mar 25, 2026

Monitoring Kinase and Phosphatase Activities Through the Cell Cycle by Ratiometric FRET

Monitoring Kinase and Phosphatase Activities Through the Cell Cycle by Ratiometric FRET

Published on: January 27, 2012

PLK-1: Angel or devil for cell cycle progression.

Shiv Kumar¹, Ashish Ranjan Sharma², Garima Sharma²

¹Department of Biochemistry, Institute of Cell Differentiation and Aging, Hallym University, College of Medicine, Chucheonsi, Gangwondo 200-704, Republic of Korea.

Biochimica Et Biophysica Acta

|February 23, 2016

Summary

This summary is machine-generated.

Polo-like kinase 1 (PLK-1) regulates the cell cycle and mitosis. Aberrant PLK-1 expression drives tumorigenesis by causing cell cycle abnormalities, making it a potential anti-cancer drug target.

Keywords:

Cell cycle progression Mitosis Mitotic kinase Polo-like kinase-1 Tumorigenesis

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Last Updated: Mar 25, 2026

Monitoring Kinase and Phosphatase Activities Through the Cell Cycle by Ratiometric FRET

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Published on: January 27, 2012

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Area of Science:

Molecular Biology
Cell Biology
Cancer Biology

Background:

Polo-like kinase 1 (PLK-1) is a critical regulator of the eukaryotic cell cycle.
Cell cycle progression is tightly controlled by specific kinases, with PLK-1 playing a key role in mitosis.

Purpose of the Study:

To review the multifaceted role of PLK-1 in cell cycle regulation.
To explore the association between PLK-1 misexpression and tumorigenesis.
To evaluate PLK-1 as a potential anti-cancer therapeutic target.

Main Methods:

Literature review of studies on PLK-1 function in cell cycle.
Analysis of research linking PLK-1 aberrant expression to cancer development.
Examination of PLK-1's role in inhibiting tumor suppressor genes like p53 and pRB.

Main Results:

PLK-1 is essential for regulating G2/M transition, mitosis, mitotic exit, and cytokinesis.
Aberrant PLK-1 expression is linked to aneuploidy and mitotic defects, promoting tumorigenesis.
PLK-1's inhibition of p53 and pRB contributes to cancer progression.

Conclusions:

PLK-1 is a crucial cell cycle regulator with a significant role in maintaining genomic stability.
Dysregulation of PLK-1 is a hallmark of many cancers, highlighting its oncogenic potential.
Targeting PLK-1 presents a promising strategy for novel anti-cancer therapies.